ラットにおける成長ホルモン分泌促進因子に対する血漿成長ホルモンの反応: 甲状腺摘除術, サイロキシン投与, 視床下部腹内側核弓状核破壊術の効果

抄録

The effect of hypo- and hyperthyroidism, and hypothalamic ventro m edial-arcuate (VMH-ARC) nuclei lesions on plasma growth hormone (GH) response to human growth hormonereleasing factor (GRF) was studied in conscious, freely moving rats after they had received chlorpromazine (CPZ) or CPZ plus antiserum against somatostatin (ASS). CPZ was chosen, since the agent is known to inhibit episodic GH secretion mediated by endogenous GRF in conscious, freely moving rats.
Following results were obtained.
1) CPZ had no effect on GH secretion induced by GRF in rat pituitary rnonolayer culture. The plasma GH response to a small dose of GRF was consistently observed in rats pretreated with CPZ alone. The magnitude of the response was significantly augmented when rats were administered with CPZ and ASS.
2) In rats made hypothyroid by thyroidectomy or hyperthyroid by the administration of 1-thyroxine, basal and the peak plasma GH response to the minimum effective dose of GRF were significantly reduced as compared to their respective controls. The pituitary GH reserve was markedly reduced in hypothyroid but not in hyperthyroid rats as compared to their controls.
3) The magnitude of plasma GH response to a moderate dose of GRF was significantly higher in VMH-ARC lesioned rats than that attained in sham lesioned rats, when the observation was made after they had received CPZ alone. When a similar observation was repeated using the same rats after they had received ASS and CPZ, basal plasma GH levels of controls were significantly higher than those of VMH-ARC lesioned rats and the magnitude of plasma GH response to GRF was augumented in both groups of rats. Under the condition, plasma GH response to GRF was comparable between the two groups, though the peak plasma GH response to GRF was slightly but significantly lower in VMH-ARC lesioned rats as compared to controls. Pituitary GH content was reduced significantly in VMH-ARC lesioned rats as compared to controls.
The results demonstrate the following :
1) CPZ acts largely if not solely to reduce endogenous GRF secretion. Therefore, rats pretreated with CPZ and ASS can be used to quantitate GRF activity.
2) Although plasma GH response to GRF is reduced in hypo- and hyperthyroidism, the mechanism involved in the phenomenon appears to be different between the two conditions.
3) The pituitary responsiveness to GRF does not appear to be altered significantly in rats bearing VMH-ARC [source of endogenous GRF] lesions. In addition, the placement of electrolytic lesions in VMH-ARC causes reduced SS secretion into hypophyseal portal vessels and leads to an augumentation of plasma GH response to GRF.